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Effects of Conditional Egfr deletion on transcriptome of the mouse cerebral cortex

ABSTRACT: Effects of Conditional Egfr deletion on transcriptome of the mouse cerebral cortex

PROVIDER: PRJNA885310 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21749741_1.fastq.gz	Fastqsanger.gz
	SRR21749741_2.fastq.gz	Fastqsanger.gz
	SRR21749742_1.fastq.gz	Fastqsanger.gz
	SRR21749742_2.fastq.gz	Fastqsanger.gz
	SRR21749743_1.fastq.gz	Fastqsanger.gz

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Effects of Conditional Egfr deletion on transcriptome of the mouse cerebral cortex

Project description:Effects of Conditional Egfr deletion on transcriptome of the mouse cerebral cortex

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Effects of Conditional Egfr deletion on transcriptome of the mouse cerebral cortex

Project description:To investigate the role of Egfr in the cerebreal cortex and hippocampal formation we conditionally deleted it using a floxed allele in combination with the Nestin-cre transgene. Cortices at E17.5 embryonic stage were harvested and split into rostral and caudal halves and RNA extracted and sequenced

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Effects of Conditional Egfr deletion on transcriptome of the mouse cerebral cortex

Project description:To investigate the role of Egfr in the cerebreal cortex and hippocampal formation we conditionally deleted it using a floxed allele in combination with the Nestin-cre transgene. Cortices at P5 post-natal stage were harvested and split into rostral and caudal halves and RNA extracted and sequenced

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Transcription profiling of mouse presenilin conditional double knockout cerebral cortex at 6 months old

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Project description:Differential gene expression of cerebral cortex might be responsible for distinct neurovascular developments between different mouse strains We used Affymetrix microarray to explore the global gene expression patterns of mouse cerebral cortex of different mouse strains at two developmental stages Cerebral cortex from two mouse strains [C57BL/6J(B6) and C3H/J (C3H)] at post-natal day 1 (p1) and post-natal 11 weeks (11 wk) were harvested for microarray experiments

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Gene expression in basal progenitors in the cerebral cortex of Tbr2 conditional knockout mice

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Expression data from mouse cerebral cortex

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Metabolomic signature of mouse cerebral cortex following Toxoplasma gondii infection

Project description:BACKGROUND: The protozoan parasite Toxoplasma gondii infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals. However, the molecules that contribute to these changes remain largely unknown.METHODS: We have investigated the impact of T. gondii infection on the overall metabolism of mouse cerebral cortex. Mass-spectrometry-based metabolomics and multivariate statistical analysis were employed to discover metabolomic signatures that discriminate between cerebral cortex of T. gondii-infected and uninfected control mice.RESULTS: Our results identified 73, 67 and 276 differentially abundant metabolites, which were involved in 25, 37 and 64 pathways at 7, 14 and 21 days post-infection (dpi), respectively. Metabolites in the unsaturated fatty acid biosynthesis pathway were upregulated as the infection progressed, indicating that T. gondii induces the biosynthesis of unsaturated fatty acids to promote its own growth and survival. Some of the downregulated metabolites were related to pathways, such as steroid hormone biosynthesis and arachidonic acid metabolism. Nine metabolites were identified as T. gondii responsive metabolites, namely galactosylsphingosine, arachidonic acid, LysoSM(d18:1), L-palmitoylcarnitine, calcitetrol, 27-Deoxy-5b-cyprinol, L-homophenylalanine, oleic acid and ceramide (d18:1/16:0).CONCLUSIONS: Our data provide novel insight into the dysregulation of the metabolism of the mouse cerebral cortex during T. gondii infection and have important implications for studies of T. gondii pathogenesis.

2020-04-23 | MTBLS770 | MetaboLights

Expression data from P7 mouse cerebral cortex and hippocampus -CTCF Nex-Cre mediated conditional knockout

Project description:The CCCTC-binding factor (CTCF) is key to chromatin conformational changes that promote cellular diversity, but nothing is known about its role in neurons. Here we produced mice with a conditional knockout (cKO) of CTCF in postmitotic projection neurons, mostly in the dorsal telencephalon. 390 transcripts were expressed at significantly different levels between CTCF-deficient and control cortex and hippocampus. 14 Total samples were analyzed. Statistical analysis was performed by ANOVA, using the core probe sets defined by Affymetrix with the revision of the clustered Pcdhs. A list of genes showing a significant difference by Ctcf deletion was generated using a false discovery rate (FDR) <0.05 with a fold difference of < -1.2 or > 1.2 as a cutoff value.

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